[Severely injured patients after the initial phase--vegetative state or remaining cognitive functions?]. / Store hjerneskader etter akuttfasen--vegetativ fungering eller bevarte kognitive funksjoner?

BACKGROUND: We wanted to quantify improvements in the subacute rehabilitation phase in patients with severe brain injuries classified as vegetative or minimal brain consciousness. MATERIAL AND METHODS: Five patients were studied during a 12 months period using a method called Coma Recovery Scale (CRS) as described by Giacino et al. (1991). The parameters measured included visual and hearing functions, motor functioning, oromotor/verbal function, communication, and arousal. The observations of the patients and commandos given were standardised in a manual, and the responses achieved from the patients were recorded according to a scale for each parameter. RESULTS: This procedure for measuring closely the progress over time in these severely brain injured patients, was used for planning a realistic rehabilitation program. It was found to be very practical in communication with relatives of the patients and with the other therapists involved. INTERPRETATION: By decomposing the cognitive functions by this method using all the available possibilities for inputs, even minimal improvement in the cognitive functions mentioned could be uncovered and recorded.

[Hypoxic brain damage after carbon monoxide poisoning. Visual agnosia, reduced initiative and memory and delayed sequelae]. / Hypoksiske hjerneskader etter forgiftning med karbonmonoksid. Visuell agnosi, nedsatt initiativ og hukommelse og forsinkede skader.

Four patients with hypoxic brain damage caused by carbon monoxide poisoning are described. Three of these had attempted suicide with car exhaust fumes. Two patients had visual agnosia due to lesions in the parieto-occipital cortex. Three patients had temporary Parkinsonian symptoms. In two of these patients CT and MRI showed lesions in the globus pallidus. They also showed reduced initiative, and in one patient this was combined with minor tics and obsessive symptoms. One patient had impaired memory as the only symptom. The patient with the longest lasting exposure developed delayed sequelae; three weeks after the poisoning he became apathetic and confused, with failing memory, Parkinsonian symptoms, and urinary and faecal incontinence. MRI showed demyelination in the periventricular white matter. His condition started to improve two months after the accident.

[Delayed symptoms of hypoxic brain damage after temporary improvement]. / Forsinkede symptomer på hypoksisk hjerneskade etter forbigående bedring.

A shipyard worker was doing welding work inside a pipe with argon as cover gas. After taking a break he fainted while controlling the weld, also inside the pipe. He was rescued after 15-20 minutes and regained consciousness after a few hours. Two days later he was discharged from hospital in apparently good health. After a week he returned to the hospital suffering from confusion, failing memory, aphasia, apraxia and urinary incontinence. MR showed elevated signal intensity bilaterally in the caudate nucleus. He improved gradually and six months later was given less demanding work. The course of his illness is consistent with delayed neuropsychiatric sequelae after hypoxia, probably due to displacement of oxygen by argon. Delayed symptoms are caused by demyelination in the subcortical white matter.

Residual urine following intermittent catheterisation in patients with spinal cord injuries.

Residual urine following catheterisation was studied using ultrasonography (Ultramark II Scientific Medical System) in 12 patients with spinal cord injury, for an average of 4 months (range 3-7 months) after the time of injury. All of the patients were examined on three occasions. Urinary tract infections were also registered, and the functional type of the urinary bladder was identified by a cystometric examination. Ultrasonography showed residual urine volumes after 25 of a total of 36 catheterisations (70%). In seven of these catheterisations the residual urine volume exceeded 50 ml, and in two patients was more than 100 ml. None of the patients had a residual urinary volume of more than 50 ml after all three catheterisations, but in all but two patients, some residual urine volume was found after at least one of the catheterisations. Low and non-significant correlations were found between residual volume and frequency of urinary tract infections. It is possible that even small residual urine volumes after catheterisations may predispose to urinary tract infections in these patients.

Team development and memory training in traumatic brain injury rehabilitation: two birds with one stone.

The need for developing team cooperation procedures when treating patients with traumatic brain injury (TBI) is stated. One approach in promoting team cooperation is to combine team development with a specific training programme. A memory training programme used in a subacute TBI rehabilitation unit is described. A combination of a team development procedure and memory training programme was performed in the unit. A questionnaire to assess team members' attitudes to team cooperation was administered before and after team development, and memory training procedures were implemented. The post-training questionnaire administration indicated a more positive perception among team members of how the team functioned. The efficacy of memory training showed variable results. The programme described may illustrate the advantages of combining a specific treatment programme with efforts to promote team development.

Self-reported social networks and interpersonal support 2 years after severe traumatic brain injury.

Fifty-four patients with traumatic brain injury (TBI) consecutively admitted to a rehabilitation hospital were examined 2 years post-injury. Social interaction and support, subjective complaints, and functional status were assessed. A large variability in social interaction and support patterns was found. Most patients had more interaction and received more support from family members than from friends and neighbours. Thirty-one patients (57.4%) reported that their social networks had markedly declined subsequent to injury. Relatively short duration of coma (< 1 week) and severe sequelae in terms of low functional status and poor emotional adjustment at follow-up, especially in terms of deficits in initiating behaviour, were found to be related to little interaction and support. The importance of both provider and patient initiative in order to establish and preserve a social support network is suggested, and clinical implications briefly discussed.

[Regaining of function following severe head injury. From primary rehabilitation to 2 years after the injury]. / Funksjonsbedring etter alvorlig hodeskade. Fra primaerrehabilitering til to år etter skade.

72 patients with sequelae after severe traumatic brain injury were studied during primary rehabilitation and two years post-injury. The patients were grouped into two main categories, one dependent as regards activities of daily living (ADL) and one mainly independent group. Most of the dependent patients, except seven low level patients close to a vegetative state, showed marked functional recovery. Among the independent patients, those who were admitted to primary rehabilitation relatively early (< 60 days post-injury) and those who were allowed a longer stay upon first admission to hospital showed better progress in functional level scores than those who were admitted later and were allowed a shorter stay during primary inpatient rehabilitation.

[Residual urine after intermittent catheterization in patients with spinal cord injuries]. / Resturin etter intermitterende kateterisering hos pasienter med ryggmargsskade.

Residual urine following catheterization was studied using ultrasonography (Ultramark II Scientific Medical System) in 12 patients with spinal cord injury, for an average of four months (range 3-7 months) after time of injury. All patients were examined three times. Urinary tract infections were also registered, and the functional type of the urinary bladder was identified by cystometric examination. Ultrasonography showed residual urine volumes after 25 of a total of 36 catheterizations (70%). In seven of these catheterizations the residual urine volume exceeded 50 ml, and in two cases was more than 100 ml. None of the patients had a residual urinary volume of more than 50 ml after all three catheterizations, but in all but two patients, some residual urine volume was found after at least one of the catheterizations. Low and non-significant correlations were found between residual volume and frequency of urinary tract infections. It is possible that even small residual urine volumes after catheterization may predispose for urinary tract infections in these patients.

[Amantadine in cognitive failure in patients with traumatic head injuries]. / Amantadin ved kognitiv svikt hos pasienter med traumatisk hodeskade.

In patients with severe cerebral injuries, attentional dysfunction may cause greater difficulties for rehabilitation than neurological deficits. These functions seem to be controlled by catecholaminergic neural systems in the central nervous system. Dopamine agonists have therefore been recently introduced in the treatment of these patients. We describe two patients treated with amantadine in daily doses of 200-400 mg. We observed improvement of cognitive functions such as visual attention, speed of information processing, attentional span, learning capacity and alertness. We stress the value of amantadine as a treatment adjuvant in patients with severe attentional deficits following injury of the brain.

[Diving of patients with spinal cord injuries]. / Dykking hos pasienter med ryggmargsskade.

Three patients with traumatic spinal cord injuries of a level below Th 5 have been certified as sports divers in Norway, and an increasing number of other paraplegics and tetraplegics have shown an interest for diving. The article reviews possible complications for these patients during diving. It is concluded that diving is not unsuitable for patients with spinal cord injuries, even for tetraplegics, but these persons run greater risk of complications than healthy divers do. However, on the basis of present knowledge, we have prohibited diving to below 20 m, and patients with spinal cord injuries over Th 5 have so far been advised not to dive. All diving must be performed only after comprehensive training and adaptation.

Chronic toxic encephalopathy among house painters with disability pension.

Among a group of 14 painters accorded a disability pension, 11 showed signs and symptoms of slight encephalopathy. Five of these 11 painters previously had been pensioned with a diagnosis of musculoskeletal disease, while the encephalopathy was unrecorded in the disability pension records. The combined effect of the two diseases may have caused the disability. We considered occupational solvent exposure the most probable cause of the encephalopathy in four of these five painters. This study indicates that case-referent studies based on diagnoses from disability pension registers may lead to underestimation of the risk of toxic encephalopathy.

Encephalopathy and polyneuropathy induced by organic solvents.

Twenty-six patients with previous heavy exposure to organic solvents were admitted to a neurological department during a 1 1/2 year period. They were studied with a battery of tests, including general medical and neurological examinations, neuropsychological tests, electroencephalography (EEG) and neurography with electromyography (EMG), and cerebral computerized tomography (CT). The presenting complaints were compatible with encephalopathy and/or polyneuropathy. When patients with alternative diagnosis were excluded, 17 patients (65%) of the initial group were diagnosed as belonging to the organic solvent syndrome. These patients had a mean time of solvent exposure of 23.9 years, ranging from one to 45 years. EEG and cerebral CT showed minor deviations only as did the neurological examination. These methods proved nevertheless of importance in excluding alternative etiologies. Neuropsychological test performances were markedly reduced, especially short-term memory. All patients were injured by occupational exposure to organic solvents, most often from painting and lacquering. Encephalopathy was a more frequent finding than polyneuropathy, and most often classified as slight or marked, whereas severe encephalopathy was not found in the present group.

Selegiline (1-deprenyl) and low-dose levodopa treatment of Parkinson's disease. A double-blind crossover trial.

Fifteen parkinsonian patients previously untreated with levodopa were treated with daily doses of 200 mg Madopar and randomized to addition of 10 mg selegiline (1-deprenyl) in a double-blind, placebo controlled, crossover trial. According to the patients own evaluations 6 reported additional therapeutic effect from selegiline to Madopar; 2 reported possible additional effect, whereas a further 6 reported no improvement; 1 did not complete the trial. Statistically significant positive therapeutic effect of selegiline could not be found on Webster's rating scale or on a sensimotoric test designed for parkinsonian disabilities. Side effects of selegiline were minimal. It is concluded that selegiline may be of some value in addition to levodopa in early treatment of parkinsonian patients, but positive therapeutic effect has to be tested individually. Even in these patients the additional therapeutic effect of selegiline to levodopa seems to be quantitatively small.

The initial phase of the dextran-induced anaphylactoid reaction in the rat: a comparison of inhibitors of the blood pressure fall.

The histamine H2-receptor antagonist cimetidine (25-100 mg/kg) caused a partial inhibition of the pronounced blood pressure fall induced by dextran (Macrodex, 40-100 mg/kg) in the rat. The inhibition by cimetidine could not be distinguished from the inhibition achieved by the serotonin D-receptor antagonist bromolysergic acid diethylamide (BOL, 1-4 mg/kg). Doses of cimetidine and BOL that gave submaximum inhibitory effects separately, showed approximately additive effects when combined. The combined effect of these drugs never exceeded the maximum effects of the drugs separately, whereas injection of tranexamic acid (AMCHA, 100-300 mg/kg) together with cimetidine or BOL, increased the total inhibition. Previous works showed that dextran injected intravenously into rats reduced the level of plasminogen (PG) and plasminogen proactivator (pro-PGA) in plasma (Briseid et al. 1979; Berstad 1980a; Berstad & Briseid 1982). High doses of AMCHA (200 mg/kg) did not inhibit these effects, but significantly increased the lowering caused by dextran of the capacity of high molecular weight kininogen (HMWK) to function as a cofactor in the activation of factor XII. BOL (1-4 mg/kg, Berstad 1981) and cimetidine (50-100 mg/kg) also reduced the cofactor capacity of HMWK in the doses that were required to provide a manifest inhibition of the dextran-induced blood pressure fall. It is suggested that the early phase of the state of shock induced by dextran in the rat can be counteracted at different sites, correlated with histamine and serotonin receptors on the one hand, and with an effect antagonized by AMCHA, on the other. The lowest effective doses of cimetidine and BOL were rather high, suggesting a less specific mechanism for their effects than inhibition at selective receptor sites.

Dextran-induced lowering of plasminogen proactivator and functionally active high molecular weight kininogen in the rat.

Incubation of plasminogen-free rat citrated plasma with acetone (23% v/v) yielded enzyme preparations with high levels of plasminogen activator (PGA) and kininogenase (kallikrein), but with a low concentration of high molecular weight kininogen (HMWK) active as cofactor for kaolin-induced activation of factor XII. When benzamidine (4.0 mM) was present during acetone activation, a high yield of functionally active HMWK was obtained. Gel chromatography separated PGA into one high molecular weight fraction (HMW-PGA) without kininogenase and BAEe esterase activity, and one fraction (LMW-PGA) eluting together with plasma kallikrein. Injection of dextran (100 mg/kg intravenously) reduced the amount of LMW-PGA to 40%, without altering the concentration of HMW-PGA, and with only a small reduction of the kininogenase activity.

Activation of factor XII in rat plasma: protection by benzamidine of the cofactor function of high molecular weight kininogen.

Factor XII has been assayed as kaolin-activated prekallikrein activator in rat citrated plasma pretreated with acetone (Briseid et al. 1978 & 1979; Briseid & Berstad 1979). In the present work benzamidine added during blood collection increased the extent of activation by a factor of 6. Rat high molecular weight kininogen (HMWK) added to acetone-treated citrated plasma likewise increased the activation, providing evidence of the protection by benzamidine of the cofactor function of HMWK. All cofactor capacity was retained after the removal of the kinin part of HMWK. Experiments carried out with plasminogen-free plasma showed that plasmin could hardly be the the factor responsible for the destruction of HMWK. The stoichiometric factor XII concentration-effect curve obtained by diluting acetone-treated rat plasma with acetone-treated human factor XII deficient plasma showed that factor XII is present in functional excess, the concentration of HMWK deciding the extent of activation. By diluting acetone-treated rat plasma with buffer, HMWK concentration-effect curves were obtained which were approximately linear over a range of 0.03-0.40 microgram (bradykinin equivalents) per ml kaolin incubate. No further activation of factor XII was obtained at 0.80 microgram/ml.